胸腺素β_4治疗脂多糖诱导小鼠内毒素休克的实验研究  

Experimental Study on Thymosin β_4 Treating Septic Shock Induced by Lipopolysaccharide

作　　者：赵裕光[1] 王爽[2] 时德[1] 

机构地区：[1]重庆医科大学附属第一医院普外科,重庆400016 [2]重庆医科大学附属第一医院神经内科,重庆400016

出　　处：《江西医学院学报》2005年第3期13-16,共4页Acta Academiae Medicinae Jiangxi

摘　　要：目的研究胸腺素β4(thymosinβ4,Tβ4)对内毒素休克小鼠72h存活率的影响,并初步探讨Tβ4治疗内毒素休克的机制。方法选用清洁级昆明小鼠腹腔注射脂多糖(LPS)制备内毒素休克动物模型,(1)观察内毒素休克前后Tβ4变化情况;(2)观察注射LPS后不同时间给予Tβ4对内毒素休克小鼠存活率的影响;(3)观察不同剂量Tβ4对内毒素休克小鼠存活率的影响;(4)ELISA法检测Tβ4对内毒素休克小鼠血浆TNFα及IL1β变化情况的影响;(5)用RTPCR的方法检测外周血单核细胞(PBMC)的TNFαmRNA及IL1βmRNA表达情况。结果Tβ4在内毒素休克小鼠的血浆中明显降低,A、B、C组内毒素休克小鼠72h存活率均明显低于D组(P<0.01,P<0.05),Tβ4预处理LPS组TNFα及IL1β血浆水平明显低于LPS组(P<0.01),LPS组TNFαmRNA及IL1αmRNA的表达明显高于Tβ4预处理LPS组(P<0.01)。结论Tβ4治疗内毒素休克应在LPS腹腔注射后0h、2h、4h连续注射Tβ4(5mg/kg),Tβ4可降低PBMC表达TNFαmRNA及IL1βmRNA。实验提示Tβ4可能是通过下调炎症介质的基因表达来治疗内毒素休克的。Objective To explore the therapeutic efficacy and its mechanism of thymosin β_4 (Tβ_4)in septic shock by observing the 72 h survival rate.Methods LPS(lipopolysaccharide)was intraperitoneally injected into clean Kunming mice to establish the animal model.(1)The T β_4 between normal and septic shock mice were determined;(2)The survival rate of septic shock mice was detected by intraperitoneal injection of Tβ_4;(3)The survival rate of septic shock mice was measured by injection of different dose Tβ_4;(4)TNF-α and IL-1β were examined in septic shock mice by ELISA;(5)The expression of TNF-αmRNA and IL-1βmRNA was measured by RT-PCR in PBMC.Results Tβ_4 was obviously decreased in the blood of septic shock mice. Tβ_4 rose the 72 h survival rate of septic shock mice and down-regulated inflammatory mediators.Conclusion The optimal protective methods in the mouse appears to be 5 mg/kg Tβ_4 given immediately following(0h)and at 2 h and 4 h successively post LPS. Tβ_4 down-regulates the inflammatory mediators,which maybe the mechanism of Tβ_4 .

关 键 词：胸腺素Β4 脂多糖 TNF-α IL—1β 动物 实验 小鼠 

分 类 号：R541.64[医药卫生—心血管疾病]